To provide direct genetic evidence for a role of IL-6 in experimental autoimmune myasthenia gravis (EAMG), IL-6 gene KO (IL-6−/−) mice in the C57BL/6 background were immunized with Torpedo californica acetylcholine receptor (AChR) and evaluated for EAMG. Only 25% of AChR-immunized IL-6−/− mice developed clinical EAMG compared to 83% of C57BL/6 (wild-type) mice. A significant reduction in the secondary anti-AChR Ab of IgG, IgG2b, and IgG2c, but not the primary or secondary IgM response was observed in AChR-immunized IL-6−/− mice, suggesting a possible defect in T cell help and class switching to anti-AChR IgG2 isotype. The AChR-specific lymphocyte proliferative response, IFN-γ, and IL-10 production were suppressed in AChR-immunized IL-6−/− mice. EAMG resistance in IL-6−/− mice was associated with a significant reduction in germinal center formation and decreased serum complement C3 levels. The data provide the first direct genetic evidence for a key role of IL-6 in the autoimmune response to AChR and in EAMG pathogenesis.
CITATION STYLE
Deng, C., Goluszko, E., Tüzün, E., Yang, H., & Christadoss, P. (2002). Resistance to Experimental Autoimmune Myasthenia Gravis in IL-6-Deficient Mice Is Associated with Reduced Germinal Center Formation and C3 Production. The Journal of Immunology, 169(2), 1077–1083. https://doi.org/10.4049/jimmunol.169.2.1077
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